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512 PART 3
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GROWTH AND DEVELOPMENT OF THE NERVOUS SYSTEM AND THE NEUROLOGY OF AGING
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motor milestones or with motor skill at a later time Children with cerebral defects tend to exhibit apathy or hyperactivity more often than children without recognizable defects Again, two groups of overactive children can be discerned In one, infants are constitutionally overactive from birth, sleeping less and feeding poorly; by the age of 2 years, the syndrome is obvious In the other group, an inability to sit quietly only becomes apparent at the preschool age (4 to 6 years) Seldom do such children remain in one position for more than a few seconds, even when watching television Attention to any task cannot be sustained, hence the term attention de cit hyperactivity disorder As a rule, there is also an abnormal impulsivity and often an intolerance of all measures of restraint Mild degrees of mental retardation and epilepsy and other disabilities are conjoined in some patients Once the child is in school, the attention de cit becomes more troubling Now these children must sit still, watch and listen to the teacher when she speaks to another child, and not react to distracting stimuli They cannot stay at their desks, take turns in reciting, be quiet, or control their impulsivity The teacher nds it dif cult to discipline them and often insists that the parents seek medical consultation A few affected children are so hyperactive that they cannot attend regular school Their behavior verges on the organic drivenness that has been known to occur in children whose brains have been injured by encephalitis In certain families the disorder is probably inherited (Biederman et al) In about half the patients, the hyperactivity subsides gradually, by puberty or soon thereafter, but in the remainder the symptoms persist in modi ed form into adulthood (Weiss et al) It has also become clear that a group of children exist who have dif culty sustaining concentration but do not manifest hyperactivity or behaviors that betray the attention de cit It is presumed that they share a similar core problem with hyperkinetic children, and it has been observed that they may be helped in studying and school performance by the same stimulant drugs that are used for the treatment of more overt ADHD For a number of years there was a tendency to consider children with the hyperkinetic syndrome as having minimal brain disease Soft neurologic signs such as right-left confusion, mirror movements, minimal choreic instability of the hands, awkwardness, nger agnosia, tremor, and borderline hyperre exia were said to be more frequent among them These signs, however, are seen so often in normal children that their attribution to disease is invalid Schain and others therefore substituted the term minimal brain dysfunction, which is no more accurate and simply restates the problem Lacking altogether are accurate clinicoanatomic and clinicopathologic correlative data Some morphologic and physiologic data are available In an MRI study of the brains of 10 children with hyperactivity attention de cit disorder, Hynd and colleagues found the width of the right frontal lobe to be smaller than normal; also fairly consistently, there was smallness of the dorsolateral, cingulate, and striatal regions Unlike dyslexics, in whom the planum temporale tends to be equal in the two hemispheres, the left planum was larger in the attention de cit cases, just as it is in normals Also, functional imaging studies have suggested that the inability of these children to block impulsive reactions and the improvement that is seen with methylphenidate are accompanied by changes in the striatum One would expect the prefrontal cortex to be implicated in such a disinhibitory syndrome but data from brain mapping in children with ADHD have been very complex and dif cult to interpret Another approach to understanding the process has been to study a strain of mice that have been genetically altered to eliminate a dopamine transporter
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gene These animals display behavioral symptoms that are said to replicate those of ADHD in children and also to respond to stimulants These observations implicate an abnormality of dopamine and serotonin; the idea is provocative because several genetic linkage studies have suggested an association between ADHD and a polymorphism of the gene that codes for the same dopamine transporter gene Apart from the reports of parents and teachers and observation of the child, one is aided in the diagnosis of the attention de cit disorder (and other learning disabilities) by psychometry An observant psychologist, in performing intelligence tests, notes distractibility and dif culty in sustaining any activity Erratic performance that is not due to a defect in comprehension is characteristic The treatment of the hyperactive child can proceed intelligently only after medical and psychologic explorations have elucidated the context in which the hyperactivity occurs If the child is hyperactive and inattentive mainly in school and less so in an unstructured environment, it may be that mental retardation or dyslexia, which prevents scholastic success, is a source of frustration and boredom The child then turns to other activities that may happen to disturb the classroom Or the hyperactive child may have failed to acquire self-control because of a disorganized home life, and the overactivity may be but one manifestation of anxiety or intolerance of constraint Clearly problems such as these require a modi cation of the educational program Treatment For overactive children of normal intelligence who have failed to control their impulses, who at all times have boundless energy, require little sleep, exhibit a wriggling restlessness (the choreiform syndrome of Prechtl and Stemmer), and manifest incessant exploratory activity that repeatedly gets them into mischief, even to their own dismay, medical therapy is in order Paradoxically, stimulants have a quieting effect on these children, whereas phenobarbital and other sedatives may have the opposite effect Methylphenidate is the drug most widely used Children under 30 kg are given 5 mg each morning on school days for 2 weeks, after which the dose can be raised to 5 mg morning and noon Children weighing less than 30 kg can be given a single 20-mg sustained-release tablet each morning If methylphenidate proves ineffective after several weeks or cannot be tolerated, dextroamphetamine 25 to 5 mg three times daily is a suitable substitute Pemoline is a weaker but sometimes better-tolerated stimulant than the others If these agents control the activity and improve school performance (they can be continued for a number of years), there is then no need to alter the child s school program If stimulants are ineffective, tricyclic antidepressants, particularly desipramine, should be tried Classroom behavioral conditioning techniques and psychotherapy may be needed for brief periods Remedial education is reserved for recalcitrant cases Certainly the disease is a lifelong problem for a proportion of children, although it is just as clear that many or most outgrow it Hill and Schoener estimate that there is a 50 percent decline in prevalence with each 5 years of growth In addition to the child with ADHD who grows to adulthood with persistent problems, there has recently emerged an interest in a group of adults who present for the rst time with features that they or their physicians attribute to ADHD Most often these adults come to realize they have had lifelong problems that are similar to the motor restlessness and wandering attention that led to the diagnosis of ADHD in their own children The ef cacy and safety of stimulant drugs in the adult group is not known with certainty, but this class of medications as well as antidepressants has been tried with some success
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